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  1. #1
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    it seems that Voltaren and Ibuprofen, popular COX-nonselective NSAIDs also promote CV pathology, just like condemned cox2-selective meds



    Risk of myocardial infarction in patients taking cyclo-oxygenase-2 inhibitors or conventional non-steroidal anti-inflammatory drugs: population based nested case-control analysis

    Julia Hippisley-Cox, professor of clinical epidemiology and general practice1, Carol Coupland, senior lecturer in medical statistics1

    1 Institution 13th floor, Tower Building, University Park, Nottingham NG2 7RD





    Correspondence to: J Hippisley-Cox Julia.hippisley-cox@nottingham.ac.uk





    Aims To determine the comparative risk of myocardial infarction in patients taking cyclo-oxygenase-2 and other non-steroidal anti-inflammatory drugs (NSAIDs) in primary care between 2000 and 2004; to determine these risks in patients with and without pre-existing coronary heart disease and in those taking and not taking aspirin.



    Design Nested case-control study.



    Setting 367 general practices contributing to the UK QRESEARCH database and spread throughout every strategic health authority and health board in England, Wales, and Scotland.



    Subjects 9218 cases with a first ever diagnosis of myocardial infarction during the four year study period; 86 349 controls matched for age, calendar year, sex, and practice.



    Outcome measures Unadjusted and adjusted odds ratios with 95% confidence intervals for myocardial infarction associated with rofecoxib, celecoxib, naproxen, ibuprofen, diclofenac, and other selective and non-selective NSAIDS. Odds ratios were adjusted for smoking status, comorbidity, deprivation, and use of statins, aspirin, and antidepressants.



    Results A significantly increased risk of myocardial infarction was associated with current use of rofecoxib (adjusted odds ratio 1.32, 95% confidence interval 1.09 to 1.61) compared with no use within the previous three years; with current use of diclofenac (1.55, 1.39 to 1.72); and with current use of ibuprofen (1.24, 1.11 to 1.39). Increased risks were associated with the other selective NSAIDs, with naproxen, and with non-selective NSAIDs; these risks were significant at < 0.05 rather than < 0.01 for current use but significant at < 0.01 in the tests for trend. No significant interactions occurred between any of the NSAIDs and either aspirin or coronary heart disease.



    Conclusion These results suggest an increased risk of myocardial infarction associated with current use of rofecoxib, diclofenac, and ibuprofen despite adjustment for many potential confounders. No evidence was found to support a reduction in risk of myocardial infarction associated with current use of naproxen. This is an observational study and may be subject to residual confounding that cannot be fully corrected for. However, enough concerns may exist to warrant a reconsideration of the cardiovascular safety of all NSAIDs.
    Man on a mission

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    This is going to change the playing field for Merck and its ongoing Vioxx litigation....
    Remember, believe none of what you hear and half of what you see...





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    I'm pretty sure this info has been well known. I read a newspaper article about this about the time the other cox2 inhibitors were pulled.

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    this research just came out and is all over the news.
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    Oh well, there's always good old aspirin.

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    Yes but NSAIDs especially Ibuprofen look particularly promising for Alzheimers and potentially over neuroinflammatory conditions involving glial activation.



    I'm just trying to think why these NSAID's would be great on the brain and bad on the heart - Nitric Oxide?



    It's the one thing that you want in the endothelial cell but not so much the neuron or neuroglia.



    Cross talk between enzymes might translate effects like that, from effects on COX, maybe?
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    ...in which case taking folic acid and perhaps arginine may help solve the problem. I recall data that Ginkyo raises eNOS but not iNOS or nNOS.
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    I think its becaue of the immune system. hampered, yu get infections all over the body. one place is the heart only there its fatal.
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    I'm not sure, what data is there for weakened immune system?



    It seems that NO is a potential means to explain these effects, the finding in the brain that expression of COX-2 lead to expression of iNOS may explain the way that Ibuprofen causes these effects. Perhaps eNOS is stunted causing increased inflammation in the cardiovaascular system, whilst it also lowers iNOS.



    This could explain why it is good for the brain and not for the heart.
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    Quote Originally Posted by ATB' post='340519' date='Jun 5 2006, 10:21 AM
    I'm just trying to think why these NSAID's would be great on the brain and bad on the heart - Nitric Oxide?


    Think horses, not zebras.



    COX-2 inhibition of vasodilator prostaglandins (PGE2, PGI2) in kidney increases the blood pressure (over time, bad for the heart).



    COX-3 is whats in the CNS, targetted best by acetaminophen. I experienced this first-hand with the nastiest flu last year, spiking crazy fevers, almost a gram of ibuprofen did nothing but 1 tylenol knocked it right down to only 1-2 degrees above normal. I would have looked in a pharmacology book sooner but I couldn't move a fucking muscle in my body.

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